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2018 ; 7
(12
): ä Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Carvacrol Attenuates Hippocampal Neuronal Death after Global Cerebral Ischemia
via Inhibition of Transient Receptor Potential Melastatin 7
#MMPMID30486272
Hong DK
; Choi BY
; Kho AR
; Lee SH
; Jeong JH
; Kang BS
; Kang DH
; Park KH
; Suh SW
Cells
2018[Nov]; 7
(12
): ä PMID30486272
show ga
Over the last two decades, evidence supporting the concept of zinc-induced
neuronal death has been introduced, and several intervention strategies have been
investigated. Vesicular zinc is released into the synaptic cleft, where it then
translocates to the cytoplasm, which leads to the production of reactive oxygen
species and neurodegeneration. Carvacrol inhibits transient receptor potential
melastatin 7 (TRPM7), which regulates the homeostasis of extracellular metal
ions, such as calcium and zinc. In the present study, we test whether carvacrol
displays any neuroprotective effects after global cerebral ischemia (GCI), via a
blockade of zinc influx. To test our hypothesis, we used eight-week-old male
Sprague?Dawley rats, and a GCI model was induced by bilateral common carotid
artery occlusion (CCAO), accompanied by blood withdrawal from the femoral artery.
Ischemic duration was defined as a seven-minute electroencephalographic (EEG)
isoelectric period. Carvacrol (50 mg/kg) was injected into the intraperitoneal
space once per day for three days after the onset of GCI. The present study found
that administration of carvacrol significantly decreased the number of
degenerating neurons, microglial activation, oxidative damage, and zinc
translocation after GCI, via downregulation of TRPM7 channels. These findings
suggest that carvacrol, a TRPM7 inhibitor, may have therapeutic potential after
GCI by reducing intracellular zinc translocation.